Gout is an independent risk factor for MI, and the increased risk of MI is present even in young people and those without cardiovascular risk factors.
IntroductionWe explored the risk of end-stage renal disease (ESRD) among gout patients in a representative cohort in Taiwan.MethodsThe primary database used was the Taiwan National Health Insurance Research Database. Subjects older than 20 years without ESRD, coronary heart disease, or stroke were included in the study. The case definition of gout in the present study was gout diagnosis and medical treatment for gout. An ESRD case was defined by the presence of chronic renal failure necessitating long-term renal replacement therapy. Multivariate Cox proportional hazards models were used to evaluate the risk of ESRD among gout patients.ResultsThe analysis included data of 656,108 patients who were followed up for a mean of 8.0 years. Among them, 19,963 (3.0%) patients had gout. At the end of 2008, 2,377 individuals (gout, n = 276; non-gout, n = 2,101) had ESRD, and 861 individuals (gout, n = 77, 27.9%; non-gout, n = 521, 24.8%) died due to ESRD. The rates of incidence of ESRD were 1.73 and 0.41 cases per 1,000 patient-years in the gout and non-gout groups. After adjustment for age, sex, and history of diabetes mellitus and/or hypertension, gout was associated with a hazard ratio (HR) of 1.57 for ESRD (95% confidence interval [CI], 1.38-1.79; P < 0.001). In patients with ESRD, the adjusted HR for death in patients with gout was 0.95 (0.74-1.23, P = 0.71), which was similar to the HR obtained in patients without gout.ConclusionsGout is associated with an increased hazard for development of ESRD.
There are few nationwide population studies on the epidemiology of rheumatoid arthritis (RA). Here, we present the epidemiologic features and mortality rates of RA in Taiwan. The catastrophic illness registry of the Taiwan National Health Insurance Research Database and the National Death Registry of Taiwan were used to estimate the incidence and prevalence of RA and its associated mortality rates. All-cause and cause-specific standardized mortality ratios (SMRs) were calculated and compared to the corresponding ratios of the general population in 2002. The study comprised 15,967 incident RA cases (3,562 men; 12,405 women) occurring from 2002 through 2007. The annual incidence of RA was 15.8 cases (men, 10.1; women, 41.0) per 100,000 population. The period prevalence was 97.5 cases (men, 37.4; women, 159.5) per 100,000 population. During 67,010 person-years of follow-up, 985 deaths (372 men; 613 women) were identified, and this corresponded to a crude mortality rate of 14.7 deaths (men, 25.0; women, 11.8) per 1,000 person-years. Compared to female patients, male patients had a higher risk for mortality (log-rank test, p < 0.001). RA patients had an SMR of 1.25 (95 % confidence interval [CI], 1.18-1.33) for all-cause mortality. Compared to the general population, RA patients of both genders in this cohort had a significantly higher risk of mortality from infection (SMR, 2.49) and gastrointestinal diseases (SMR, 1.76). RA incidence and prevalence were higher in women than in men. Mortality was higher in men than in women. Compared to the general population, RA patients had a higher risk of death, particularly from infection and gastrointestinal diseases.
Little is known about hepatitis B virus (HBV) diversity changes within a host during the immunotolerant phase of chronic HBV infection. Such knowledge, nevertheless, may help in understanding how host immunity and HBV interact at the early stage of infection. In this study, serial serum samples were collected from a long-term (>17 years) follow-up cohort of seven patients, and multiple copies of the full-length viral genome from serially sampled sera were recovered and analyzed. Viral genetic diversity was positively correlated with host immunity, represented by levels of alanine aminotransferase (ALT), but was negatively correlated with the viral copy number. During the immunotolerant phase, when the host immunity was feeble (ALT < 20 U/liter), viral nucleotide diversity decreased while copy numbers increased. Rates of evolutionary change derived for different patients were in a very narrow range (1.6 ؋ 10 ؊5 to 5.4 ؋ 10 ؊5 /site/year). As the disease progressed toward the immunoclearance phase (ALT > 20 U/liter), viral diversity increased but copy numbers decreased. Evolutionary rates varied among patients in accordance with their levels of ALT, ranging from 9.6 ؋ 10 ؊6 to 3.2 ؋ 10 ؊4 /site/year. More than half (19/32 sites) of positively selected sites resided in immune epitopes, suggesting their possible role in host immunity. Our results demonstrate that host immunity is a dominant factor in HBV evolution. Different selective forces, including immune-mediated positive selection and virus-mediated negative selection, operate in tandem in shaping viral population dynamics within a host.
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